P0035URINARY CITRATE AS A MARKER OF RENAL FUNCTION IN PATIENTS WITH AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE. (6th June 2020)

• Record Type: Journal Article
• Authors: Borrego-Utiel, Francisco-Jose; Herrera, Isidoro; Merino Garcia, Enoc; Moriana Dominguez, Clara; Camacho Reina, Victoria; Ocaña Perez, Esther
• Is Part Of: Nephrology dialysis transplantation. Volume 35(2020)Supplement 3
• Publication Date: 2020-06-06
• Subjects: Nephrology -- Periodicals; Hemodialysis -- Periodicals; Kidneys -- Transplantation -- Periodicals; Hemodialysis; Kidneys -- Transplantation; Nephrology; Periodicals; 616.61
• DOI: 10.1093/ndt/gfaa142.P0035
• Languages: English
• ISSNs: 0931-0509

Abstract

Abstract: Background and Aims: In autosomal dominant polycystic kidney disease (ADPKD) is frequent to find low urinary citrate levels. Recently it has been suggested that urinary citrate could be a marker of covert metabolic acidosis. Our aim was to analyze relationship between urinary citrate levels and renal functionality in ADPKD patients. Method: We determined citrate, calcium and uric acid in 24-hour collected urine from 91 ADPKD patients Results: Urinary citrate/creatinine ratio was 214±158 (range 5.3-678) mg/g Cr with levels significantly higher in females. When considering chronic kidney disease (CKD) stages we observed a progressive decrease in urinary osmolality and in urinary citrate, calcium and uric acid elimination. Low levels of citrate (<300 mg/g Cr) were present in 40% in CKD-1 stage, in 69.7% in CKD-2 stage, 92% in CKD-3 stage and 100% in CKD-4 + 5 stages. Urinary citrate was correlated with serum creatinine (r= -0.66, p<0.001) and eGFR (r= 0.56, p<0.001). Urinary citrate significantly correlated with urinary calcium but correlation with urinary uric acid was weaker. We did not find any correlation with serum bicarbonate. Using multiple lineal regression analysis we found as predictors of urinary citrate to glomerular filtration rate, female gender and urinary calcium levels. In a subgroup of patients we measured total kidney volume and we found an inverse correlation with urinary citrate levels that dissappeared when it was corrected with glomerular filtration rate. We did not also find a relationship between urinary elimination of calcium or uric acid and TKV after adjusting with eGFR. Conclusion: Urinary citrate is very frequently reduced in ADPKD patients being present from very early CKD stages. Their levels are inversely correlated with glomerular filtration rate and directly with urinary calcium excretion. We did not found a relathionship with serum bicarbonate. We think that it would be interesting to study urinary citrate in other nephropathies and verify if it could be a marker of covert metabolic acidosis.